Efforts are directed towards the prevention or control of graft- versus-host disease in human allogeneic bone marrow transplantation. Since graft-versus-host disease is mediated by alloreactive T cells in the inoculated marrow, reagents and techniques have been developed to remove these T cells from the marrow inoculum. Murine monoclonal antibodies specific for antigens expressed on human T cells in marrow. By a new limiting dilution assay, residual T cells in marrow following depletion are at a level less than 0.01% of the total cell population. A bank of such T cell depleted, characterized marrows has been generated for use in the therapy of human malignancy. The potential of such T cell depleted marrow to successfully hematologically and immunologically reconstitute a host has been examined in murine models. The role of T cells in the infused marrow and the susceptibility of host rejecting cells to radiation and monoclonal antibodies administered in vivo are also under study. Within the T cell population, the fine specificity of human CTL has been demonstrated to be sufficient to distinguish among alpha 1 and 2 domain changes of class I major histocompatibility complex molecules. Such human cytotoxic T cells have been further studied with respect to cell surface molecules utilized in their interactions with target cells as the basis for therapeutic interventions with the intent of preventing tissue damage mediated by such allo-reactive cytotoxic T cells. It has been shown that inhibition by a monoclonal antibody with specificity for CD18 occurs in the absence of target cells thereby raising the possibility that this inhibition is independent of cell-cell adhesion. Further studies have identified the site of this inhibition as involving cell surface molecule interaction or the T cell receptor associated G protein. This in vitro generated information has been applied to bone marrow transplantation models in monkey and swine. Utilizing T cell depleted marrow, extended solid organ allograft survival (without exogoneous immunosuppression), but not long term tolerance induction, can be achieved in primates.